An estrogen-responsive animal model (ovariectomized rat, maintained with estradiol-benzoate) has been used to study mediators involved in estradiol-induced uterine hyperemia (EIUH). We have shown that an intact alpha-receptor is needed for the elicitation of the response, and that a beta-receptor-mediated system inhibits the response at high doses of estrogen. Pharmacologic studies have shown that histamine is not involved in the early EIUH. The uterine paracervical ganglion appears to be necessary for elicitation of EIUH. However, radioenzymatic assay has shown to change in uterine catecholamines during EIUH, and pharmacologic studies have shown that functional adrenergic nerves are not essential to the response. It is postulated that the numerous norepinephrine-containing chromaffin cells of the uterine paracervical ganglion may be the source of the alpha stimulant which is activated during EIUH, and that their catecholamine reaches the uterus by a non-neuronal route. BIBLIOGRAPHIC REFERENCES: Williamson, H.E., Marchand, G.R., Bourland, W.A., Farley, D.B., Van Orden, D.E., Ethacrynic Acid Induced Release of Prostaglandin E to Increase Renal Blood Flow Prostaglandins (in press, 1976). Baker, H.A., Clark, K.E., Brody, M.J., Bhatnagar, R.K., Van orden, D.E., and Van Orden, III, L.S., Effect of Paracervical Ganglionectomy on Estrogen induced Uterine Hyperemia in the Rat. Fed. Proc. 35 (3): 457, 1976.